| First Author | Seavitt JR | Year | 1999 |
| Journal | Mol Cell Biol | Volume | 19 |
| Issue | 6 | Pages | 4200-8 |
| PubMed ID | 10330160 | Mgi Jnum | J:55023 |
| Mgi Id | MGI:1337148 | Doi | 10.1128/mcb.19.6.4200 |
| Citation | Seavitt JR, et al. (1999) Expression of the p56(Lck) Y505F mutation in CD45-deficient mice rescues thymocyte development. Mol Cell Biol 19(6):4200-8 |
| abstractText | Mice deficient in the transmembrane protein tyrosine phosphatase CD45 exhibit a block in thymocyte development. To determine whether the block in thymocyte development was due to the inability to dephosphorylate the inhibitory phosphorylation site (Y505) in p56(lck) (Lck), we generated CD45-deficient mice that express transgenes for the Lck Y505F mutation and the DO11.10 T-cell antigen receptor (TCR). CD4 single-positive T cells developed and accumulated in the periphery. Treatment with antigen resulted in thymocyte apoptosis and the loss of transgenic- TCR-bearing cells. Peripheral CD45-deficient T cells from the mice expressing both transgenes responded to antigen by increasing CD69 expression, interleukin-2 production, and proliferation. These results indicate that thymocyte development requires the dephosphorylation of the inhibitory site in Lck by CD45. |
